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Clinic Director, Pittsford Performance Care
Pittsford, New York, USA
Web Version. Clinical Case Review. 2025.
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Download PDFPersistent post concussion symptoms represent a significant clinical challenge, particularly when symptoms extend years beyond the initial injury despite extensive medical evaluation and treatment. While acute concussion management pathways are well established, post acute and chronic presentations often lack clear guidance once imaging and standard neurological testing appear normal.
This case review describes a patient presenting five years after a concussive and whiplash injury with persistent cognitive, affective, vestibular, and musculoskeletal symptoms. The case highlights how functional neurological assessment may reveal clinically meaningful deficits in the absence of structural pathology and how targeted, adaptive care may influence symptom trajectory even years after injury.
A 28-year-old female presented for evaluation seeking relief from chronic muscle tightness and pain. Further consultation revealed a history of a concussive and whiplash injury sustained after falling down stairs approximately five years prior. The initial impact was described as occurring at the tailbone with force transmission through the spine, followed by cervical acceleration and deceleration.
Following the injury, the patient developed progressive and persistent symptoms including decreased drive, apathy, daily headache, neck pain, back pain, head pressure, mental fog, severe fatigue, and impaired short-term recall. Over the ensuing five years, she underwent multiple pharmacological and non-pharmacological interventions without meaningful or sustained improvement. At presentation, frustration was high and the patient expressed concern that full recovery was no longer attainable.
Initial imaging performed following the injury was unremarkable, and no pathological neurological signs were documented during acute care. As a result, evaluation emphasized functional neurological assessment rather than structural pathology.
A comprehensive bedside neurological examination was conducted with focus on cortical, subcortical, vestibular, cerebellar, and autonomic domains. Findings demonstrated multiple soft neurological deficits suggestive of reduced activation and coordination across distributed neural pathways. These included vestibulo-ocular reflex dysfunction, asymmetric cerebellar coordination, bradykinetic upper extremity movement patterns, and signs consistent with increased sympathetic tone.
The pattern of findings did not align with a single focal neuroanatomical lesion, supporting the clinical impression of a centrally mediated functional suppression process, potentially influenced by ongoing neurogenic inflammation.
Based on clinical history and examination findings, the patient was assessed as having persistent post concussion syndrome complicated by centrally mediated vestibular dysfunction and suspected neurogenic inflammation. This framework provided a unifying explanation for the patient's cognitive, affective, vestibular, and musculoskeletal symptoms rather than treating each complaint in isolation.
A three-week, multimodal neurological rehabilitation program was initiated and delivered on site. Care was receptor-driven and designed to influence cortical and subcortical activation patterns through targeted sensory and motor inputs.
Treatment emphasis was placed on adaptability rather than rigid protocol application. Frequent reassessment was performed to monitor neurological response and guide progression of care. Nutritional and dietary recommendations were also provided to support systemic recovery and reduce inflammatory burden.
At re-examination following completion of care, previously observed functional neurological deficits demonstrated marked improvement. Vestibulo-ocular reflex performance normalized, cerebellar coordination became symmetric, and bradykinesia resolved.
From a patient-reported perspective, the individual described near-complete resolution of primary symptoms including headache, head pressure, cognitive fog, fatigue, affective flattening, musculoskeletal pain, and tremors. Improvements were reported as sustained at follow-up and accompanied by restoration of confidence in daily function and quality of life.
This case illustrates that persistent post concussion symptoms may reflect functional suppression within neural networks rather than irreversible structural injury. In such cases, absence of pathological findings does not necessarily indicate neurological normalcy.
Functional neurological assessment can provide clinically actionable insight even years after injury, and adaptive care strategies may require frequent modification as neural metabolic capacity improves. This underscores the importance of individualized assessment and outcome-guided decision making in complex post acute neurological presentations.
This publication describes a single observational case and does not establish generalizable treatment efficacy. Outcomes reflect an individual response to care and should not be interpreted as predictive for all patients with similar clinical presentations.
This case aligns with the clinical philosophy of Pittsford Performance Care, which emphasizes individualized neurological assessment, adaptability of care delivery, and outcome-driven clinical reasoning. It reinforces the value of functional evaluation in patients with persistent symptoms following concussion when standard diagnostic pathways fail to explain ongoing impairment.
The patient described her experience at Pittsford Performance Care as highly supportive and structured after years of unsuccessful treatment attempts elsewhere. She emphasized clear communication, careful monitoring of her responses to care, and appreciation for understanding the rationale behind each phase of treatment. The patient reported a meaningful restoration of quality of life following completion of care.
This case review is provided for educational purposes only. It does not constitute medical advice, clinical guidelines, or treatment recommendations. Content reflects a de-identified retrospective observation from clinical practice and is not intended to establish generalizable clinical evidence.
No external funding was received for the development of this material.